Comparative analysis of the hspA mutant and wild-type Synechocystis sp. strain PCC 6803 under salt stress: evaluation of the role of hspA in salt-stress management.

Abstract

DNA microarray analysis has previously revealed that hspA, which encodes a small heat-shock protein, is the second most highly expressed gene under salt stress in Synechocystis sp. strain PCC 6803. Consequently, an hspA deletion mutant was studied under various salt stresses in order to identify a potential role of HspA in salt stress management. The mutant had a growth disadvantage under moderate salt stress. It lost the ability to develop tolerance to a lethal salt treatment by a moderate salt pre-treatment when the tolerance was evaluated by cell survival and the level of major soluble proteins, phycocyanins, while the wild-type acquired tolerance. Under various salt stresses, the mutant failed to undergo the ultrastructural changes characteristic of wild-type cells. The mutant, which showed higher survival than the wild-type after a direct shift to lethal salt conditions, accumulated higher levels of groESL1 and groEL2 transcripts and the corresponding proteins, GroES, GroEL1, and GroEL2, suggesting a role for these heat-shock proteins in conferring basal salt tolerance. Under salt stress, heat-shock genes, such as hspA, groEL2, and dnaK2, were transcriptionally induced and greatly stabilized, indicating a transcriptional and post-transcriptional mechanism of acclimation to salt stress involving these heat-shock genes.